Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of harmful substances (bacteria, toxins and antigens) present within the intestinal lumen. At birth, the newborn infant must be prepared to deal with bacterial colonization of the gut, with formation of toxic byproducts of bacteria and viruses (enterotoxins and endotoxins) and with the ingestion of antigens (milk proteins). These potentially noxious substances if allowed to penetrate the mucosal epithelial barrier under pathological conditions can cause inflammatory and allergic reactions which may result in gastrointestinal and systemic disease states. To combat the potential danger of invasion across the mucosal barrier the infant must develop an elaborate system of defence mechanisms within the lumen and on the luminal mucosal surface which act to control and maintain the epithelium as an impermeable barrier to uptake of macromolecular antigens. These defences include a unique immunological system adapted to function in the complicated milieu of the intestine as well as other non-immunological processes such as a gastric barrier, intestinal surface secretions, peristaltic movement and natural antibacterial substances (lysozyme, bile salts) which also help to provide maximum protection for the intestinal surface. Unfortunately, during the immediate postpartum period, particularly for premature and small-for-dates infants, this elaborate local defence system is incompletely developed. As a result of the delay in the maturation of the mucosal barrier newborn infants are particularly vulnerable to pathological penetration by harmful intraluminal substances. The consequences of altered defence are susceptibility to infection and the potential for hypersensitivity reactions and for formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis and hepatitis. Fortunately, 'nature' has provided a means for passively protecting the 'vulnerable' newborn against dangers of a deficient intestinal defence system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leucocytes but many other substances which can interfere with bacterial colonization and prevent antigen penetration.
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PMID:Gastrointestinal host defence: importance of gut closure in control of macromolecular transport. 26 21

The most apparent immunologic role of the mammary gland is supply to antibodies to the neonate. In cattle the gland must be able to secrete large quantities of IgG antibodies over a short time period to supply the offspring with protection against systemic pathogens. This is accomplished by selective transfer of IgG from serum to the gland followed by eventual absorption by the neonate gut. In all mammals, the mammary glands provide IgA antibodies specific for pathogens or antigens which enter or invade the neonatal gut. An entero-mammary cell circulation provides the mechanism for conveying such specificity to the lacteal IgA antibodies. Some IgA antibodies may also be derived from the circulation so that the quantitative significance of serum derived versus locally produced IgA in different species requires clarifications. IgG and IgG lacteal antibodies ingested by the neonate, provide short-term systemic and long-term enteric humoral immunity to the neonate. In addition to providing passive immunity, at least swine IgG appears to have a regulatory role in the development of the systemic humoral immune system of the neonate. Such a phenomenon may be general for IgG antibodies transferred in colostrum or in utero. While passive antibodies and immunoglobulins may be most important for the neonate, the many other potentially anti-infectious elements transferred in colostrum and milk may also play important roles. 'Bifidus' factor particularly, but also lysozyme and lactoferrin are probably all important although more convincing experimental data will be needed to support this assumption. Studies of cells of the lymphoid and reticuloendothelial systems in milk are more recent and their role in the neonate remains to be convincingly demonstrated. In summary, the immunologic and anti-infectious roles of the mammary glands are (1) Supply of IgA antibodies against enteric antigens to the neonate on a 'long-term' basis throughout lactation; (2) Short-term supply of IgG (and IgA) in Group II and III mammals for eventual absorption into neonatal serum; (3) The supply of numerous nonspecific factors such as 'bifidus factor,' lactoferrin, and lysozyme throughout lactation; (4) Regulation of the development of humoral immunity by an apparent feedback mechanism involving maternal IgG; (5) Self-protection of the gland by sensitized T-lymphocytes acting directly or using lymphokines on macrophages; and (6) Self-protection of the gland by secreted antibodies that may act in complement-independent cytolysis, as opsoins for polymorphonuclear-leukocytes or directly as agents preventing colonization.
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PMID:Immunologic aspects of breast feeding, antiinfectious activity of breast milk. 39 68

In patients with Crohn's disease and ulcerative colitis, alterations in serum storage temperature produced significant changes in serum lysozyme activity (SLA) as measured by the lysoplate method. This was not the case in healthy controls or in a group with other gastrointestinal disorders. Electrophoretic separation of serum revealed two components of lysozyme-type lytic activity but only one in extracts of gut mucosa, leucocytes, and egg white. The major lytic component of serum migrated towards the cathode and reacted with specific antilysozyme serum, but the minor component which migrated towards the anode did not. Although the cause of this anionic lytic activity is uncertain, it contributes to total serum activity as estimated by any method utilising the lysis of Micrococcus lysodeikticus, and may possibly be related to the observed thermolability.
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PMID:Complex nature of serum lysozyme activity: evidence of thermolability in inflammatory bowel disease. 62 14

The effect of bile acids on the bacteriolytic activity of lysozyme towards Micrococcus lysodeikticus was studied in vitro. All bile acids tested inhibited lysozyme activity. Conjugated bile acids were better inhibitors than their unconjugated homologs and sulfation resulted in still stronger inhibition. A study of UV-difference spectra of bile acid-lysozyme mixtures suggests that bile acids distort the tertiary structure of the enzyme. The inhibition-concentration curves of micelle-forming bile acids were bell-shaped, and peak inhibition was apparently related to the critical micellar concentration. The inhibition-concentration curves of sulfated bile acids, which do not form micelles, are characterized by a plateau of maximal inhibition. A mechanism of lysozyme activation by bile acid micelles is proposed. Our results illustrate the complex interactions between antibacterial compounds in the gut. As bile acids are known to inhibit lipase activity as well, these studies suggest that bile acids may have an important influence on intestinal enzyme activity in general.
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PMID:The inhibition of lysozyme by bile acids. 94 95

Changes in the activities of three gastric and nine pancreatic enzymes plus colipase were determined during postnatal development and weaning in calves. In calves exclusively milk-fed for 2, 7, 28, 56, 70 and 119 d, the enzyme activities per kilogram of empty live weight increased with age for chymotrypsin, elastase, carboxypeptidases A and B, ribonuclease and alpha-amylase, decreased for chymosin, lysozyme and colipase but showed no change in the case of pepsin, trypsin, lipase and phospholipase A2 compared with animals at birth. The greatest increase was that in alpha-amylase activity (about 50-fold between d 2 and 119). In calves weaned between d 28 and 56, all the activities were higher than in milk-fed animals, except that of chymosin (which was slightly lower) and that of colipase (which did not change). At 119 d of age, chymotrypsin, carboxypeptidase A, alpha-amylase and lipase were 1.6- to fourfold higher in ruminants than in preruminants. Thus, most enzyme activities were modified first by colostrum and milk intake, and again upon weaning by development of the forestomachs and ingestion of solid food. These ontogenic patterns might be under the control of many gut regulatory peptides, the plasma concentrations of which changed simultaneously. Some gastric and pancreatic enzymes were correlated to plasma concentrations of these gut regulatory peptides.
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PMID:Gastric and pancreatic enzyme activities and their relationship with some gut regulatory peptides during postnatal development and weaning in calves. 137 46

Riboprobe in situ hybridization (rISH) demonstrates active lysozyme synthesis in ulcerative colitis and Crohn's disease. Maximal labeling was seen in Paneth cells, macrophages, and granulomas. Diffuse infiltration of the mucosa by lysozyme-rich polymorphs characterizes ulcerative colitis but obscures reactivity in other cell lineages in immunohistochemical studies; lysozyme mRNA is not detected in polymorphs, rISH giving a clearer picture than immunohistochemical studies of the active synthesis of lysozyme within the gut in inflammatory bowel disease. In ulcerative colitis, strong signals localized to Paneth cell metaplasia were found in 11 of 20 cases and to a lesser degree in non-Paneth cell lineages in regenerative mucosa in 13 of 20 cases. In Crohn's disease, abundant labeling was seen in tuberculoid granulomas (5 of 20) and over macrophage aggregates in the lamina propria in another 7, characteristic patterns not encountered in ulcerative colitis. Low levels of lysozyme messenger RNA were found in the ulceration-associated cell lineage ("pseudopyloric metaplasia"). These results support the view that neutrophils are largely responsible for elevated fecal lysozyme levels in ulcerative colitis and macrophages for elevated serum lysozyme levels in Crohn's disease.
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PMID:Lysozyme gene expression in inflammatory bowel disease. 163 71

Low levels of lysozyme were found in the midgut epithelium of the tobacco hornworm, Manduca sexta, during the early part of the fifth larval stadium. This was observed in control insects as well as in bacterially challenged insects. No lysozyme was detected in the gut contents of either group of insects which were actively eating or in the early stages of metamorphosis. However, high levels of lysozyme activity were detected in homogenates of midgut tissue collected from insects later in the stadium. Immunocytochemical studies demonstrated that lysozyme accumulates in large apical vacuoles in regenerative cells of the midgut during the larval-pupal molt. These cells, initially scattered basally throughout the larval midgut epithelium, multiply and form a continuous cell layer underneath the larval midgut cells. At the larval/pupal ecdysis the larval midgut epithelium is sloughed off and the regenerative cells, now forming the single cell layer of the midgut, release the contents of their vacuoles into the midgut lumen. This release results in high lysozyme activity in the lumen of the pupal midgut and is thought to confer protection from bacterial infection. This is the first indication that the lysozyme gene may be developmentally regulated in a specific tissue in the absence of a bacterial infection.
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PMID:Lysozyme in the midgut of Manduca sexta during metamorphosis. 180 32

The equine Paneth cell response to a shift in the microbial balance of the intestinal tract was studied by inducing an acute episode of alimentary laminitis in 6 mature ponies. The normal bacterial population of the gut was modified by administration of a carbohydrate-rich ration. During acute laminitis a dramatic degranulation of the Paneth cells occurred in the intestinal glands throughout the duodenum, jejunum, and ileum. Bacteriocidal lysozyme, which was immunohistochemically identified as a component of the Paneth cell secretory granule, was evident in the glandular lumina and in degranulated Paneth cells. These results indicate that lysozyme is secreted by the equine Paneth cell in an apparent attempt to regulate the changing microbial population induced by carbohydrate overload of the gut. From these observations, it is suggested that the Paneth cell plays a role in the mucosal defense system of the equine intestinal tract.
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PMID:Paneth cell degranulation and lysozyme secretion during acute equine alimentary laminitis. 186 51

The aim of this study was to optimise conditions for mRNA detection by nonisotopic in situ hybridisation (NISH) using biotinylated and digoxigenin labelled riboprobes. Because lysozyme gene transcripts are present at high concentrations in Paneth and other alimentary cells, archival gut biopsy specimens were chosen as a model system for these experiments. Most of the variables in NISH, from unmasking of mRNA, to its ultimate detection by peroxidase or alkaline phosphatase based detection systems, were examined in detail. The most important findings were that simultaneous heating of tissue targets and riboprobes at 95 degrees C for 15 minutes before hybridisation at 50 degrees C for two hours gave the most intense signal for lysozyme mRNA in Paneth cells, Brunner's glands, and lamina propria macrophages; digoxigenin labelled riboprobes gave a higher signal to noise ratio than their biotinylated counterparts, and probes 600 base pairs long were superior to shorter probes. It is concluded that the mRNA NISH method may be generally useful for detecting gene transcription in archival clinical biopsy specimens.
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PMID:Model system for optimising mRNA non-isotopic in situ hybridisation: riboprobe detection of lysozyme mRNA in archival gut biopsy specimens. 196 Feb 17

Immunohistological assessment of Kupffer cells was made using the antibody MAC387 and an antibody to lysozyme. Autopsy liver samples from 13 fetuses aged from 17 weeks gestation to term, and from 10 neonates and children aged 1 day to 18 months, were studied. For comparison, 10 normal adult autopsy liver specimens were included. The number of positively staining cells per unit area was counted for periportal sinusoids (zone 1) and centrilobular sinusoids (zone 3). No difference was found between zone 1 and zone 3 macrophage numbers with either antibody at any stage of development. Hepatic sinusoidal macrophage numbers were low during early gestation but increased during intra-uterine life to reach approximately normal adult values in the neonatal period. The numbers of cells staining with MAC387 or lysozyme were similar in each case except for hepatic sinusoidal macrophages in fetuses of less than 30 weeks gestation. Here anti-lysozyme stained significantly fewer cells, suggesting that lysozyme production may be low in immature fetuses. No difference was found between infants of similar maturity who had died immediately or had lived for more than 48 h and hence been exposed to gut antigens.
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PMID:Kupffer cell numbers during human development. 239 14


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